Management of Coronary Vascular Disorders

1,132 views

Published on

0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total views
1,132
On SlideShare
0
From Embeds
0
Number of Embeds
5
Actions
Shares
0
Downloads
37
Comments
0
Likes
0
Embeds 0
No embeds

No notes for slide

Management of Coronary Vascular Disorders

  1. 1. Management of Patient with Coronary Vascular Disorders Chapter 28
  2. 2. Coronary Artery Disease (CAD) <ul><li>Most prevalent type of CVD in adults </li></ul><ul><li>Decreased blood flow through coronary arteries = myocardial ischemia/infarction </li></ul><ul><li>Ischemia results from insufficient O2 supply to myocardium </li></ul><ul><li>Atherosclerosis is leading contributor </li></ul>
  3. 3. CAD <ul><li>Describe common manifestations of Coronary Artery Disease. </li></ul><ul><li>Discuss risk factors for CAD. </li></ul><ul><ul><li>Modifiable </li></ul></ul><ul><ul><li>Non-modifiable </li></ul></ul><ul><li>Describe Coronary Artery Disease Risk Equivalents. </li></ul>
  4. 4. Atherosclerosis <ul><li>Describe the pathophysiology of atherosclerosis. </li></ul><ul><li>Review Figure 28-1, p. 860 </li></ul>
  5. 5. Acute Coronary Syndromes <ul><li>Serious manifestation of CAD </li></ul><ul><li>Amount of disruption of the plaque determines the degree of obstruction of the coronary artery and specific disease process: </li></ul><ul><ul><ul><li>Unstable angina </li></ul></ul></ul><ul><ul><ul><li>Non-ST elevation MI </li></ul></ul></ul><ul><ul><ul><li>ST elevation MI </li></ul></ul></ul>
  6. 6. Angina Pectoris <ul><li>“ Strangling of the chest” </li></ul><ul><li>Imbalance between O2 supply and demand </li></ul><ul><li>Compare and contrast Stable and Unstable Angina Pectoris. </li></ul><ul><li>Describe associated clinical manifestations. </li></ul>
  7. 7. Angina Pectoris-- Management <ul><li>Medical Management </li></ul><ul><li>Pharmacologic therapy </li></ul><ul><ul><li>Nitroglycerin </li></ul></ul><ul><ul><li>Beta-adrenergic blockers </li></ul></ul><ul><ul><li>Calcium channel blockers </li></ul></ul><ul><ul><li>Antiplatelets </li></ul></ul><ul><ul><li>Anticoagulants </li></ul></ul><ul><li>Oxygen therapy </li></ul><ul><li>Nursing Management </li></ul><ul><li>Treat associated symptoms </li></ul><ul><ul><li>Immediate rest </li></ul></ul><ul><ul><li>Oxygen </li></ul></ul><ul><ul><li>assessment </li></ul></ul><ul><ul><li>ECG </li></ul></ul><ul><ul><li>Nitroglycerin </li></ul></ul><ul><li>Reduce anxiety </li></ul><ul><li>Prevent pain </li></ul>
  8. 8. Myocardial Infarction <ul><li>When does a myocardial infarction occur? </li></ul><ul><li>What degree of blood flow reduction results in ischemia? </li></ul><ul><li>What will occur if blood flow is not restored to the myocardium? </li></ul><ul><li>What is the most common cause of coronary artery occlusion? </li></ul><ul><li>What are other causes? </li></ul>
  9. 10. Process of Infarction <ul><li>Dynamic process that evolves over several hours </li></ul><ul><li>Normal conduction and contractile functions are suppressed </li></ul><ul><li>Automaticity and ectopy are enhanced </li></ul><ul><li>Heart rate and force of contraction are increased </li></ul><ul><li>Oxygen requirements increase </li></ul>
  10. 11. Physiologic Response to Infarction <ul><li>Will take up to six hours for obvious changes to occur in the heart (blue and swollen) </li></ul><ul><li>After 48 hours (gray with yellow streaks) </li></ul><ul><li>By 8-10 days granulation tissue forms at edges of necrotic tissue </li></ul><ul><li>Within 2-3 months scarring develops which changes the shape of the left ventricle (ventricular remodeling) </li></ul><ul><li>Remodeling may ↓ L ventricular function, cause heart failure, and ↑ morbidity and mortality </li></ul>
  11. 12. MI Assessment: History <ul><li>Query patient about chest pain </li></ul><ul><ul><li>If experiencing acute chest discomfort, delay history and treat discomfort </li></ul></ul><ul><li>Obtain information about </li></ul><ul><ul><li>Management of current episode of discomfort </li></ul></ul><ul><ul><li>Current medications </li></ul></ul><ul><ul><li>Family history of CAD </li></ul></ul><ul><ul><li>Presence of modifiable risk factors </li></ul></ul>
  12. 13. MI Assessment: Pain <ul><li>Must differentiate type of chest discomfort and identify source </li></ul><ul><li>Query patient to determine characteristics of discomfort </li></ul><ul><ul><li>Onset </li></ul></ul><ul><ul><li>Location </li></ul></ul><ul><ul><li>Radiation </li></ul></ul><ul><ul><li>Intensity </li></ul></ul><ul><ul><li>Duration </li></ul></ul><ul><ul><li>Precipitating and facilitating factors </li></ul></ul>
  13. 14. MI Assessment: Pain <ul><li>Remember: </li></ul><ul><ul><li>angina is ischemic pain and usually improves when oxygen supply/demand disparity resolves. </li></ul></ul><ul><ul><li>MI does not usually resolve with simple measures </li></ul></ul><ul><li>Associated symptoms: nausea, vomiting, diaphoresis, dizziness, weakness, palpitations, and shortness of breath </li></ul>
  14. 15. MI Assessment: Cardiovascular <ul><li>Blood pressure </li></ul><ul><li>Heart rate </li></ul><ul><li>Cardiac rhythm </li></ul><ul><li>Distal peripheral pulses </li></ul><ul><li>Skin temperature </li></ul><ul><li>Heart sounds </li></ul><ul><li>Respiratory rate </li></ul><ul><li>Breath sounds </li></ul>
  15. 16. MI Assessment: Psychosocial <ul><li>Denial is common early reaction </li></ul><ul><ul><li>Can be normal part of adapting to stressful event </li></ul></ul><ul><ul><li>Detrimental if denial interferes with identification of symptom </li></ul></ul><ul><li>Other common reactions </li></ul><ul><ul><li>Fear </li></ul></ul><ul><ul><li>Anxiety </li></ul></ul><ul><ul><li>anger </li></ul></ul>
  16. 17. MI: Laboratory Assessment <ul><li>Cardiac Enzymes </li></ul><ul><ul><li>Creatine kinase (CK) </li></ul></ul><ul><ul><li>CK-MB isoenzyme </li></ul></ul><ul><li>Myoglobin </li></ul><ul><ul><li>Found in serum 2-3 hours after MI, but is not cardiac specific </li></ul></ul><ul><ul><li>Always increases within 3-6 hours after MI, if not increased at 6 hour mark can rule out MI </li></ul></ul><ul><li>Troponin T and I </li></ul><ul><li>Increased WBC </li></ul>
  17. 18. Cardiac Markers for MI <ul><li>Creatine Kinase (CK) </li></ul><ul><li>Cardiac enzyme released after injury </li></ul><ul><li>Levels rise 3-12 hours after acute MI </li></ul><ul><li>Levels peak in 24 hours </li></ul><ul><li>Levels to normal within 2-3 days </li></ul><ul><li>MB band is specific to myocardial cells </li></ul><ul><ul><li>>3% indicates MI </li></ul></ul>
  18. 19. Cardiac Markers for MI <ul><li>Troponin </li></ul><ul><li>Myocardial muscle protein released after injury </li></ul><ul><li>Two subtypes: T and I </li></ul><ul><li>Greater sensitivity and specificity for myocardial injury </li></ul><ul><li>Levels rise in 3-12 hours after MI </li></ul><ul><li>Levels peak in 24-48 hours </li></ul><ul><li>Levels back to baseline over 5-14 days </li></ul><ul><li>Used for diagnostic purposes in conjunction with CK and the MB fraction </li></ul>
  19. 20. Acute MI: Other Diagnostic Tests <ul><li>ECG </li></ul><ul><li>Stress Test </li></ul><ul><li>Thallium scans </li></ul><ul><li>MRI </li></ul><ul><li>Cardiac catheterization </li></ul><ul><li>(Discussed in Chapter 26) </li></ul>
  20. 21. ECG Changes in MI <ul><li>ST-segment elevation </li></ul><ul><li>T-wave inversion </li></ul><ul><li>Abnormal Q wave </li></ul>
  21. 22. Acute MI: Collaborative Problems <ul><li>Acute Pulmonary Edema </li></ul><ul><li>Heart Failure </li></ul><ul><li>Cardiogenic Shock </li></ul><ul><li>Dysrhythmias/Cardiac Arrest </li></ul><ul><li>Pericardial Effusion and Cardiac Tamponade </li></ul>
  22. 23. Acute MI: Interventions <ul><li>Pain Management: </li></ul><ul><li>Nitroglycerin </li></ul><ul><li>Morphine Sulfate </li></ul><ul><li>Supplemental O 2 </li></ul><ul><li>Position of Comfort </li></ul><ul><li>Quiet and calm environment </li></ul>
  23. 24. Acute MI: Interventions <ul><li>Thrombolytics </li></ul><ul><li>Fibrinolytics dissolve clots and restore myocardial perfusion </li></ul><ul><li>Most effective when given within 6 hours of onset of MI </li></ul><ul><li>Client must be continuously monitored </li></ul><ul><li>Contraindications: Table 41-3, p. 850 </li></ul><ul><li>During administration monitor for bleeding and report any signs to physician </li></ul>
  24. 25. Acute MI: Interventions <ul><li>Thrombolytics (cont) </li></ul><ul><li>Post administration observe closely for signs of bleeding by: </li></ul><ul><ul><li>Documenting neuro status </li></ul></ul><ul><ul><li>Observing IV sites </li></ul></ul><ul><ul><li>Monitoring clotting studies </li></ul></ul><ul><ul><li>Observing for s/s of internal bleeding </li></ul></ul><ul><ul><ul><li>Monitor Hemoglobin and Hematocrit </li></ul></ul></ul><ul><ul><li>Testing stools, urine, emesis for occult blood </li></ul></ul>
  25. 26. Acute MI: Interventions <ul><li>Glycoprotein (GP) Inhibitors </li></ul><ul><ul><li>Target platelet component of the thrombus </li></ul></ul><ul><ul><li>Prevent fibrinogen from attaching to activated platelets at the site of a thrombus </li></ul></ul><ul><ul><li>Used in: </li></ul></ul><ul><ul><ul><li>Acute coronary syndromes </li></ul></ul></ul><ul><ul><ul><li>During and before PCTA to ensure patency </li></ul></ul></ul><ul><ul><ul><li>Conjunction with fibrinolytics following MI </li></ul></ul></ul><ul><ul><li>During administration nurse assesses closely for bleeding or hypersensitivity reactions </li></ul></ul>
  26. 27. Acute MI: Interventions <ul><li>Drug Therapy </li></ul><ul><li>ASA </li></ul><ul><li>Beta-adrenergic blocking agent </li></ul><ul><li>ACE inhibitors </li></ul><ul><li>Calcium channel blockers </li></ul>
  27. 28. Acute MI: Interventions <ul><li>Cardiac Care Rehabilitation </li></ul><ul><li>Process which assists client with cardiac disease to achieve and maintain optimal functioning within the limits of the heart’s ability to respond to increases in activity and stress </li></ul><ul><ul><li>Phase 1: begins with acute illness, ends with discharge from hospital </li></ul></ul><ul><ul><li>Phase 2: begins after discharge and continues through convalescence at home </li></ul></ul><ul><ul><li>Phase 3: long term conditioning </li></ul></ul>
  28. 29. Acute MI: Interventions <ul><li>Cardiac Care Rehabilitation Phase 1 </li></ul><ul><li>Nurse promotes rest while ensuring some limited mobility </li></ul><ul><li>Assistance is given for some ADL’s </li></ul><ul><li>Individualized– client’s progress at their own rate </li></ul><ul><li>Nurse encourages progressive ambulation </li></ul><ul><li>Nurse assesses heart rate, BP, respiratory rate and level of fatigue with each higher level of activity </li></ul><ul><li>Nurse should stop the activity and refrain from advancing activity if client develops any signs of activity intolerance </li></ul>
  29. 30. Acute MI: Interventions <ul><li>Coping </li></ul><ul><li>During acute phase antianxiety agents may be prescribed </li></ul><ul><li>Nurse assesses current coping mechanisms </li></ul><ul><ul><li>Most common are denial, anger and depression </li></ul></ul><ul><ul><ul><li>Denial which allows the client to minimize threat and use problem-focused coping mechanisms may be helpful in decreasing anxiety </li></ul></ul></ul><ul><ul><ul><li>Anger may represent an attempt to regain control of life </li></ul></ul></ul><ul><ul><ul><li>Depression may be the response to grief and loss of function </li></ul></ul></ul>
  30. 31. Dysrhythmias <ul><li>Cause of death in clients with MI who die prior to hospitalization </li></ul><ul><li>70-90% of hospitalized MI clients have abnormal cardiac rhythms </li></ul><ul><ul><li>Identify the dysrhythmia </li></ul></ul><ul><ul><li>Assess hemodynamic status </li></ul></ul><ul><ul><li>Evaluate client for chest discomfort </li></ul></ul><ul><li>Treated when they cause </li></ul><ul><ul><li>Hemodynamic compromise </li></ul></ul><ul><ul><li>Increased myocardial oxygen requirements </li></ul></ul><ul><ul><li>Predispose lethal ventricular dysrhythmias </li></ul></ul>
  31. 32. Dysrhythmias <ul><li>Inferior MI </li></ul><ul><ul><li>Bradycardias </li></ul></ul><ul><ul><li>2nd Degree AV Blocks </li></ul></ul><ul><ul><li>Transient </li></ul></ul><ul><ul><li>Nurse monitors: </li></ul></ul><ul><ul><ul><li>Cardiac rate & rhythm </li></ul></ul></ul><ul><ul><ul><li>Hemodynamic status </li></ul></ul></ul><ul><ul><li>May need temporary pacer if hemodynamically unstable </li></ul></ul><ul><li>Anterior MI </li></ul><ul><ul><li>Venrticular irritability (PVCs) </li></ul></ul><ul><ul><li>3rd Degree or Bundle Branch Block (serious complication) </li></ul></ul><ul><ul><li>Nurse observes closely for s/s of heart failure </li></ul></ul><ul><ul><li>May need pacemaker </li></ul></ul>
  32. 33. PTCA: Percutaneous Transluminal Coronary Angioplasty <ul><li>Invasive, but nonsurgical technique to reduce frequency and severity of chest discomfort </li></ul><ul><ul><li>Complexity and location assessed to determine whether client would benefit from procedure </li></ul></ul><ul><ul><li>May also be used during evolving MI </li></ul></ul><ul><li>Procedure performed under fluoroscopic guidance in cardiac cath lab </li></ul><ul><ul><li>Balloon inflation may be repeated until lesion is reduced or eliminated </li></ul></ul><ul><ul><li>Meds include: heparin, nitriglycerine or nifedipine </li></ul></ul><ul><ul><li>Stents may be placed at time of procedure </li></ul></ul>
  33. 34. PTCA: Post-Procedure Care <ul><li>Monitor for potential problems </li></ul><ul><ul><li>Acute closure of the vessel </li></ul></ul><ul><ul><li>Bleeding from insertion site </li></ul></ul><ul><ul><li>Reaction to the dye </li></ul></ul><ul><ul><li>Hypotension </li></ul></ul><ul><ul><li>Hypokalemia </li></ul></ul><ul><ul><li>dysrhythmias </li></ul></ul><ul><li>Drug Therapy </li></ul><ul><ul><li>Long term nitrate </li></ul></ul><ul><ul><li>Calcium channel blockers </li></ul></ul><ul><ul><li>ASA </li></ul></ul><ul><ul><li>Beta blocker and ACE inhibitor may be added </li></ul></ul><ul><ul><li>Glycoprotein inhibitors during initial hours </li></ul></ul><ul><ul><li>Potassium supplements if indicated </li></ul></ul><ul><ul><li>Coagulation with coumadin </li></ul></ul>
  34. 35. Coronary Artery Bypass Graft <ul><li>Most common cardiac surgery </li></ul><ul><li>Indicated for clients who do not respond to medical management of CAD or when disease progression is evident </li></ul><ul><li>To be bypassed vessels should have proximal lesions with > 70% occlusion </li></ul><ul><li>Most effective when good ventricular function remains and ejection fraction is more than 40-50% </li></ul><ul><li>Requires Cardiopulmonary bypass during surgery </li></ul>
  35. 36. CABG: Post-Op Care <ul><li>Mechanical ventilation for 3-6 hours </li></ul><ul><li>Mediastinal tubes to waterseal drainage </li></ul><ul><li>Epicardial pacing wires </li></ul><ul><li>Hemodynamic monitoring </li></ul><ul><li>Observes closely for: </li></ul><ul><ul><li>Dysrhythmias (ventricular ectopics, bradydysrhythmias, or heart block) </li></ul></ul><ul><ul><li>Fluid and electrolyte imbalances (K+ at 4-5) </li></ul></ul><ul><ul><li>Hypotension, hypothermia, hypertension </li></ul></ul><ul><ul><li>Cardiac tamponade </li></ul></ul><ul><ul><li>Altered cerebral perfusion </li></ul></ul>
  36. 37. Cardiac Tamponade <ul><li>Blood accumulates around the heart </li></ul><ul><li>Medical emergency </li></ul><ul><li>Hallmarks in post-CABG patient: </li></ul><ul><ul><li>Sudden cessation of previously heavy mediastinal drainage </li></ul></ul><ul><ul><li>JVD with clear lung sounds </li></ul></ul><ul><ul><li>Pulsus paradoxus </li></ul></ul><ul><ul><li>Equalization of PAWP and right artrial pressure </li></ul></ul>
  37. 38. Neurological Changes Post-CABG <ul><li>Transient: </li></ul><ul><li>75%; transient changes due to: </li></ul><ul><ul><li>Anesthesia, CPB, air emboli, hypothermia </li></ul></ul><ul><li>Experience: </li></ul><ul><ul><li>Slowness to arouse </li></ul></ul><ul><ul><li>Memory loss </li></ul></ul><ul><ul><li>confusion </li></ul></ul><ul><li>Usually return to baseline in 4-8 hours </li></ul><ul><li>Permanent </li></ul><ul><li>Changes may be associated with stroke during surgery </li></ul><ul><li>Experience: </li></ul><ul><ul><li>Abn. pupillary response </li></ul></ul><ul><ul><li>Failure to awaken from anesthesia </li></ul></ul><ul><ul><li>Seizures </li></ul></ul><ul><ul><li>Absence of sensory or motor function </li></ul></ul><ul><li>Monitor: </li></ul><ul><ul><li>Neuro status q 30-60 min initially then q 2-4 hours </li></ul></ul>

×